ARTICLE

Neural Aspects of Muscle Stretching

Nathalie Guissard and Jacques Duchateau
Laboratory of Applied Biology and Research Unit in Neurophysiology, Universite Libre de Bruxelles,
Brussels, Belgium

GUISSARD, N., and J. DUCHATEAU. Neural aspects of muscle stretching. Exerc. Sport Sci. Rev., Vol. 34, No. 4,
pp. 154Y158, 2006. Neural mechanisms contribute significantly to the gains that occur in the range of motion about a joint with
stretching exercises. In the acute condition, lengthening of a muscle-tendon unit decreases spinal reflex excitability, which reduces passive
tension and increases joint range of motion. Similarly, participation in a stretch-training program decreases tonic reflex activity and
increases flexibility. Key Words: stretch training, passive torque, reflex activity, presynaptic inhibition, postsynaptic inhibition

INTRODUCTION to the progressive increase in the passive torque of the

Flexibility of the tissues about a joint can influence the
amplitude and economy of a movement. In sports, muscle
stretching is common because of the inherent constraints of
the muscle-tendon units and joint range of motion in
executing technical movements that require extreme motion
at some joints. In rehabilitation, stretching is used as a
method to maintain or regain the range of motion of a joint
that is necessary for movements performed during daily
activity. Current opinion acknowledges that acute muscle
stretching and long-term stretch training generate both
mechanical adaptations of the muscle-tendon unit and neural
adjustments in the spinal circuitry. The objective of this
review is to examine the neural mechanisms that accompany
acute muscle stretching and long-term stretch training.
ACUTE EFFECT OF MUSCLE STRETCHING
In isolated muscle from animals, it has been shown that
slow or static stretching of the muscle-tendon unit induces
acute changes in its passive length-tension relation (14).
This effect is nonlinear during dynamic loading because of
the contribution of the viscoelastic properties of the tissues
Address for correspondence: Dr. Nathalie Guissard, Laboratory of Applied Biology,
Universite Libre de Bruxelles, 28 Avenue P. Heger, CP 168, 1000 Brussels, Belgium
(E-mail: nguissar@ulb.ac.be).
Accepted for publication: April 26, 2006.
Associate Editor: Roger M. Enoka, Ph.D.
0091-6331/3404/154Y158
Exercise and Sport Sciences Reviews
Copyright * 2006 by the American College of Sports Medicine
muscle-tendon unit. Structures such as muscle fascicles
(structural proteins), tendons, aponeurosis, joint capsules,
and ligaments contribute to limit the range of motion that
can be achieved with passive muscle lengthening. In vivo,
however, the amount of stretch that can be produced is
attributable to muscle resistance caused by tonic reflex
activity (1,11).
Effects of Static Stretching on Reflex Activity
Passive stretching refers to the technique of lengthening a
muscle group by slowly moving a joint to its maximal range
of motion and maintaining the position for a period (usually
910 s). Contrary to fast muscle lengthening, static stretch-
ing does not increase reflex activity of the stretched muscle,
but instead reduces spinal reflex excitability. This inhibition
can be tested in the soleus muscle by recording the
Hoffmann reflex (H reflex) and the tendon reflex (T reflex)
by means of electromyography. The H reflex is induced by
the stimulation of the Ia fibers of the tibial nerve in the
popliteal fossa (13), whereas percussion of the Achilles
tendon with a reflex hammer is used to produce the T reflex.
The H-reflex amplitude can be modulated at two levels: the
motor neuron and the Ia synaptic transmission (presynaptic
inhibition). The presynaptic Ia inhibitory pathways project
presynaptically through one or more interneurons onto the
Ia terminals. Hence, the amplitude of the H reflex can be
modulated by presynaptic inhibition without any changes in
motor neuron excitability (4). In contrast, the amplitude of
the T reflex is influenced by both the adjustments that
occur in the neural circuitry (motor neuron excitability and
presynaptic inhibition) and by changes in the sensitivity of
the muscle spindle. Therefore, in addition to slight differ-
ences in the monosynaptic and oligosynaptic contributions
to the H and T reflexes, the comparison of the relative

154

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changes in the amplitudes of both reflex responses allows
one to identify the contribution of the spindle to the
observed changes during a stretch.
This comparison was performed in the soleus muscle
during static stretching by progressively moving the ankle
joint in increments of 5- (7). In such conditions, the
amplitude of the H reflex decreased more than the amplitude
of the T reflex (j31% of control value for the H reflex
compared with j8% of control value for the T reflex). The
amplitudes of the T and H reflexes remain depressed as long
as the stretching maneuver was maintained (Fig. 1). Overall,
the decline in both reflex responses indicates that the
magnitude of the change in muscle length influences the
magnitude of the reduction in spinal reflex excitability during
muscle stretching (7). After the stretching maneuver, the
amplitude of the H reflex returned immediately to its control
value, whereas the amplitude of the T reflex remained below
its control value. These results suggest that the reduction in
the amplitude of the T reflex did not result from changes
located in the neural circuitry but was likely caused by either
a reduction in muscle spindle sensitivity or increased
compliance of the muscle-tendon unit. The decrease in both
T and H reflexes was not associated with significant changes
in the maximal compound action potential of the muscle
(Mmax) that was evoked by supramaximal electrical stimu-
lation of the motor nerve. This stability of the Mmax
response ensured that the stimulation conditions remained
constant throughout the experiments.
Inhibitory Mechanisms During Static Stretching
The structure of the human muscle-tendon unit is
characterized by thixotropic properties, which indicates that
the stiffness and viscosity of the system depend on the pre-
ceding activity of the muscle (14). Some receptors, such as
muscle spindles, also display thixotropic behavior and thus
discharge differently according to the immediate history of
Figure 1. Change in the amplitude of the maximal direct motor re-
sponse (Mmax), H reflex, and T reflex in the soleus muscle as a function
of the ankle dorsiflexion (left part of the graph) and during 10 minutes of
stretching at maximal dorsiflexion (right part of the graph). Data are
expressed as percentages of control values (ankle in neutral position: 0-).
R (recovery) indicates the end of the stretching maneuver. Asterisk
reflects a value that is significantly different from the control value. Data
were compiled from Guissard et al. (7). H reflex indicates Hoffmann
reflex; T reflex, tendon reflex; R, recovery.
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Number 4
October 2006
Copyright @ 2006 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
length change and the type of conditioning contraction. For
example, the stretch sensitivity of primary spindle endings is
increased after the muscle has been held at long lengths
compared with short lengths (6). Muscle stretching induces
adjustments that can be of peripheral origin by exerting an
action on the receptor (muscle spindle, Golgi tendon organ)
or of central origin by influencing the neural circuitry. A
decrease in the amplitude of the H reflex during passive
stretching suggests that neural changes are induced by the
stretch and contribute to muscle lengthening by reducing the
afferent input to the motor neuron pool and therefore
reducing tonic reflex activity. The decline in the H-reflex
amplitude, however, may involve multiple neural mecha-
nisms that are located at presynaptic and postsynaptic sites.
To study changes in excitability of the soleus motor neuron
pool during muscle lengthening, Delwaide (4) recorded a
spinal reflex response in a pathway devoid of presynaptic
inhibitory inputs. A train of stimuli delivered to the posterior
tibial nerve at the ankle induced a reflex response that
originated mainly from cutaneous nerve fibers that project
polysynaptically onto the same motor neuron pool (extero-
ceptive or E reflex; Fig. 2A). By comparing the H reflex and
the E reflex, Delwaide (4) demonstrated that for small-
amplitude passive stretches, induced by a thrust against the
Achilles tendon, the size of the H reflex decreased without
any change in the E reflex. A systematic investigation of the
H and E reflexes during small-amplitude stretches of the
ankle confirmed that presynaptic mechanisms contribute to
the decrease in the amplitude of the H reflex (8). This
conclusion was supported by the observation that neither the
E reflex nor the motor evoked potentials (MEPs) induced by
transcranial magnetic stimulation changed when the H
reflexes were decreased (8) (Fig. 2). For large-amplitude
stretches (910- dorsiflexion), both reflexes (H and E) and
MEP decreased similarly, suggesting that postsynaptic inhibi-
tory mechanisms contribute to the observed changes. Again,
this inhibition was transient, as both reflex and MEP
responses returned to control values within a few seconds
after the end of the stretching maneuver.
Thus, the decrease in reflex loop activity during small-
amplitude stretching (G10- dorsiflexion) is likely attribut-
able to presynaptic inhibition of the Ia afferents without
changes in motor neuron excitability. It is also possible that
homosynaptic depression (a decrease in synaptic activity
because of a reduced capacity for synaptic transmission from
the Ia afferents to the motor neurons) may contribute to the
presynaptic inhibition (2). However, because homosynaptic
depression lasts approximately 12 s, and the recording of the
two reflexes began at least 20 to 30 s after the onset of the
passive stretching, this mechanism likely did not play a
major role in the reduction in the amplitude of the H reflex.
Furthermore, when subjects exerted a maximal voluntary
contraction of the triceps surae muscle during a stretching
protocol, the size of the H reflex recovered completely,
suggesting that the active inhibitory mechanism was under
the control of the nervous system.
The decrease in MEP size during large-amplitude stretch-
ing (910- ankle dorsiflexion) could be due to reduced excit-
ability of both the cortical neurons and > motor neurons.
The observation of a concurrent and similar decrease in
Muscle Stretching 155
 Figure 2. (A), Experimental setup for the H and E reflexes
recording in the soleus muscle and the different pathways
involved: (1) Ia afferent, including presynaptic inhibitory inter-
neuron; (2) cutaneous afferent; (3) > motor axon; and (4) cor-
ticospinal tract. Comparison of the changes in the H reflex (B), E
reflex (C), and MEP (D) in all subjects as a function of the ankle
dorsiflexion. Data are expressed as percentages of the control
value (ankle in neutral position: 0-), after the normalization of
each response with respect to the corresponding Mmax. The
average value is represented by a continuous line, and each
dashed line denotes the data for one subject. Asterisk indicates
that the value is significantly different from the control value.
Data were compiled from Guissard et al. (8). PSI indicates pre-
synaptic inhibitory interneuron; MEP, motor evoked potential.

MEP and E reflex responses during large-amplitude stretching located at both presynaptic and postsynaptic sites. Presy-
suggests a reduced excitability of the motor neuron pool naptic mechanisms dominate during small-amplitude
through spinal postsynaptic inhibitory mechanisms. Different stretches, whereas postsynaptic mechanisms contribute more
spinal inhibitory mechanisms, such as afferent input from the to reflex inhibition during large-amplitude stretches.
Golgi tendon organs and Renshaw cells, can reduce motor
neuron excitability during muscle stretching. The afferents Inhibitory Mechanisms During Different Methods
from joint and cutaneous receptors do not seem to play a of Stretching
major role in the inhibition of the spinal reflex excitability. Muscle stretching performed at slow velocities appears to
The Golgi tendon organs primarily respond to the force of be more effective than rapid and repetitive movements (11)
a contraction and are less sensitive to the mechanical because the former avoids reflex responses from the
tension of passive stretching. They appear to be activated stretched muscles. Some years ago, proprioceptive neuro-
only during large-amplitude stretching. In humans, a pure Ib muscular facilitation (PNF) techniques were designed to
inhibition of soleus motor neurons can be elicited by the inhibit reflex activities and thereby reduce passive muscle
electrical stimulation of group I fibers in nerve to the medial resistance during stretching maneuvers. Since that time, a
gastrocnemius muscle, as it is not contaminated by any Ia number of studies have shown that PNF techniques increase
excitation. The resulting heteronymous Ib inhibition of the
soleus motor neuron pool lasts less than 10 ms. The con-
ditioning stimulation of the nerve to medial gastrocnemius
reduces the amplitude of the soleus H reflex because of the
heteronymous inhibition by the excitation of the Ib fibers
(12). The conditioned H reflex is decreased by 32.3% when
the ankle is in a neutral position (0- of dorsiflexion). At 10-
and 20- of dorsiflexion, however, the conditioning stimulus
was less effective, and the decline in the amplitude of the H
reflex corresponded to 9 and 3.4%, respectively (Fig. 3).
These results suggest that by increasing the level of
dorsiflexion, postsynaptic inhibition onto the motor neurons
pool is progressively augmented, and thereby, the contribu-
tion of heteronymous inhibitory afferents to the motor
neuron pool of the soleus muscle is progressively weakened.
In addition to the contribution of the Golgi tendon organs Figure 3. Bar graph showing the change in H reflex (hatched bars) and
to postsynaptic inhibition of the motor neuron pool during the conditioned H reflex (filled bars) recorded in a neutral ankle position
large-amplitude stretches, recurrent inhibition via the (0-) and during muscle stretching (10- and 20- of ankle dorsiflexion) in the
Renshaw loop may also contribute to the reduction in the soleus muscle of eight subjects. The H reflex was conditioned by a weak
stimulation (below motor threshold) of the nerve to medial gastrocnemius
amplitude of the H reflex. delivered 4 to 6 ms before the H-reflex response was triggered.
In conclusion, the reduction in the excitation of motor Conditioned vs unconditioned H reflex: ***P G 0.001. H reflex indicates
neurons during muscle stretching is caused by mechanisms Hoffmann reflex; Cond. H reflex, conditioned H reflex.

156 Exercise and Sport Sciences Reviews www.acsm-essr.org

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Figure 4. Changes in the relation between ankle joint position and
passive torque produced by the plantar-flexor muscles during the course of a
30-d stretch-training program. Passive torque is expressed as percentage of
the maximal torque produced during the greatest ankle dorsiflexion tolerated
by the subject in the pretraining test. The curves, fitted by exponential
equation (r2 9 0.99), are recorded before (open circles) and after 10 (open
triangles), 20 (open inverted triangles), and 30 (filled circles) sessions of
stretch training. The SEM is shown for maximal dorsiflexion. Significant
difference from pretraining values: *P G 0.05; **P G 0.01; ***P G 0.001.
(Reprinted from Guissard, N., and J. Duchateau. Effect of static stretch
training on neural and mechanical properties of the human plantar-flexor
muscles. Muscle Nerve 29:248Y255, 2004. Copyright * 2004 John Wiley &
Sons, Inc. Used with permission.)
the range of motion of a joint more effectively than passive
stretching (7). The PNF techniques often involve static
stretching used in combined procedures: either preceded by a
maximal isometric contraction of the muscle (contract-relax,
CR) or accompanied by a maximal isometric contraction of
the antagonistic muscle (antagonist-contract, AC).
When static stretching is preceded by a maximal vol-
untary contraction of the muscle to be stretched, the length
of the muscle usually increases more than when the stretch
is not preceded by a maximal contraction (7). In addition
to a possible reduction in the compliance of the elastic
components following the isometric contraction, neural
changes also contribute to the increased range of motion.
The duration of the preceding contraction is not critical as
the amplitude of the H reflex decreases by a similar
proportion immediately after maximal contractions of the
triceps surae ranging from 1 to 30 s (7). Furthermore, the re-
duction in H-reflex amplitude is not influenced by the
magnitude of the contraction that precedes the stretching
maneuver. Indeed, Enoka et al. (5) observed a similar
reduction in H-reflex amplitude for voluntary contractions
performed at 50 and 100% of the subjects maximal capacity.
The decrease in excitability of the spinal reflex recorded
after the isometric contraction is brief (G5 s) but appears to
be long enough to provide an advantage for a subsequent
stretching maneuver. The mechanisms responsible for this
transient hypoexcitability are probably located at the
presynaptic level (6). In addition, possible reduction in
muscle stiffness immediately after the maximal voluntary
contraction, the advantage of the CR method over the static
stretching method, results from the benefit of postcontraction
inhibition of the motor neuron pool.
When static stretching is associated with a contraction of
the antagonistic muscle, the mechanisms related to recip-
Volume 34
Number 4
October 2006
Copyright @ 2006 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
rocal inhibition can be added to those considered previ-
ously. Although opposite results have been obtained for the
hamstrings muscles (11), the AC method increases the
inhibition of the motor neurons that belong to the muscle
being stretched and allows a greater muscular extensibility
(3). For both stretching techniques (CR and AC), the H
reflex returns immediately to the initial level of excitability
regardless of the duration of the stretch.
LONG-TERM EFFECT OF STRETCH TRAINING
Few studies have investigated the mechanisms of adaptation
to chronic muscle stretching. In the past, studies mainly focused
on the effect of stretch training on the range of motion or
passive torque (15). The reduction in passive torque recorded
at a given muscle length after a program of stretch training has
been attributed to changes in the compliance of the tendon,
the connective tissues, and myofibrils. In addition, the
increased joint range of motion after training has been
attributed to an increase in the tolerance to stretch (10).
To determine the contribution of neural and mechanical
mechanisms to the limitations in the range of motion about a
joint, we examined the effects of a 6-week training program of
static stretch training (10 min/d) of the triceps surae (9). The
training program produced an increase in the ankle dorsi-
flexion range of motion of 30.8%, with 56% of the gain
attained after only 10 sessions. Thirty days after the end of
the training program, 74% of the gain in ankle dorsiflexion
remained. The training program progressively shifted the
torque-angle relation toward a reduced passive stiffness of the
muscle-tendon unit (Fig. 4). For all subjects, there was a
significant positive relationship between the gain in ankle
dorsiflexion and the reduction in passive stiffness (r2 = 0.88;
P G 0.001). These results suggest that an increase in the
compliance of the muscle-tendon unit in a relaxed state after
training may be attributable to either a change in viscoelastic
properties or a decrease in reflex stiffness.
As observed during acute stretching, tonic reflex activity
appears to decline after a stretch-training program, potentially
Figure 5. Bar graphs showing the change in Tmax/Hmax ratio during the
course of a 30-d stretch-training program. Data, expressed in absolute values,
are means T SEM for 12 subjects. Significant difference from pretraining
values: *P G 0.05. Data were compiled from Guissard and Duchateau (9).
Muscle Stretching 157
contributing to the observed decrease in passive torque.
Consistent with this hypothesis, the amplitude of the H and
T reflexes declined significantly during the course of the
training program. However, the T-reflex amplitude decreased
to a greater extent (36 vs 14%) and more rapidly than the H
reflex, reaching significant values after 20 training sessions.
The greatest decline in the H reflex was only observed after 30
training sessions. The reduction in the amplitude of the H
reflex suggests that motor neuron excitability was decreased or
that synaptic transmission from Ia afferents to the motor
neuron pool was reduced after stretch training.
An alternative possibility is that there was a reduction in
tonic Ia (facilitatory) afferent feedback from muscle spindles
as the maximal amplitude of the T reflex (Tmax) also
declined during the training program. This reduction in T-
reflex amplitude after training could be related to a reduced
sensitivity of the muscle spindles or an increased compliance
of the passive elastic components of the muscle-tendon unit.
In the latter case, the tendon tap would have been less
effectively transmitted to the muscle spindles. However, our
data show that the decline of the amplitude of the T reflex
did not parallel the reduction in passive stiffness during
the stretch-training program. Furthermore, the decrease
in the Tmax/Hmax ratio (Fig. 5), which measures changes
in the sensitivity of the muscle spindle and tendon stiffness,
is not correlated (P 9 0.05) with changes in passive stiffness
after 10, 20, or 30 training sessions (9). These results indicate
that the decrease in passive stiffness of the muscle-tendon unit
cannot entirely account for the decrease in T-reflex (Tmax)
amplitude and that spinal reflex excitability is intrinsically
reduced after stretch training. This conclusion is also
supported by the observation that Tmax recovered to its
pretraining values before passive stiffness. Collectively, these
results suggest that the neural input to the motor neuron pool
is reduced after 30 sessions of stretching and partly contributes
to the gain in flexibility.
SUMMARY AND FUTURE DIRECTION
Both mechanical and neural factors influence the response
to stretching. The increased flexibility during a prolonged
stretch results mainly from reduced passive stiffness of the
muscle-tendon unit. Because passive resistance is attributable
to both intrinsic stiffness and neural mechanisms (15), changes
at both levels can increase the flexibility around a joint.
Proprioceptive neuromuscular facilitation techniques can
increase flexibility, but the underlying neural mechanisms
and efficacy with long-term use are unknown. The initial
changes that are produced by stretch training involve me-
158 Exercise and Sport Sciences Reviews
Copyright @ 2006 by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited.
chanical adaptations that are followed by neural adaptations,
which contrasts with the sequence observed during strength
training. The timing of these adaptations and their relative
contributions to the gains in range of motion about different
joints remain largely unexplored.
Acknowledgments
The authors are particularly grateful to Dr. Carol Mottram for useful
comments on the paper and to A. Desseir for assistance in the preparation
of the manuscript. This study was supported by the Universite Libre de
Bruxelles and the Fonds National de la Recherche Scientifique of Belgium.
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